Who needs calcium supplementation?
Let us restrict our discussion to post menopausal women.
Let us be sure that our patients are not Vitamin D or calcium deficient (sub-clinical or clinical
Now, who needs supplementation?
Calcium in the body can remain in two forms, Ionic and Hydroxyapatite.
Ionic form is in the serum is about 1% and its serum level is fixed at 8.5 – 10.5mgm% (a range
of 2mgm). This will remain constant as long as possible and may be at the expense of bone.
Hormones are constantly working to maintain it namely Parathyroid, and Calcitonin. Parathyroid
respond to low serum ionic calcium and Calcitonin respond to high calcium level in the serum.
The hydroxyapatite constitutes 99% total body calcium and is found in the bones.
The menopausal lady is losing calcium in the urine. This loss is supposed to be due to
excessive resorption. There is increased osteoclastic activity due to diminished level of
Where this calcium supplementation will go?
There is a direct relationship between Osteoporosis and aortic vessels calcification.
This aortic vessels calcification is a slow process. Deposition in to coronary vessels is what is
feared in the article published in the BMJ.
The proposed calcium supplementation in menopausal lady is on assumption that there is state
of sub-clinical hypocalcaemia, to which parathyroid responds by increase secretion and there is
further increased osteoclastic activity to mobilize calcium from the bone to correct this presumed
hypocalcaemia in the serum. This perpetual reaction ends in a net loss of calcium.
Menopausal lady is losing calcium in urine, hence need supplementation. This calcium
supplementation is given to prevent secondary hyperparathyroidism. This is logically not correct.
The hypocalcaemic state or the increase levels of parathyroid hormones have never been
diagnosed in the lab at any time in menopausal females. This is all hypothetical.
Who can retain calcium?
Is it possible for the body to retain any calcium which is not required by the body?
Not a nanogram will stay in the body if not required as it is against the principle of energy
conservation. The serum ionic calcium will not increase or cannot increase due to tight control of
hormones. The hydroxyapatite in the bone will not form as there is no relatively increased
osteoblastic activity (compare to osteoclastic activity).
Menopausal ladies have two choices at menopause, either gain weight or lose it.
This is basically dependent on the thyroid functions. Hypothyroids gain weight and hyper
thyroids lose weight. The thyroid functions are disturbed at menopause and it will in the direction
selected by genetics. Here genetics play a big role. The hypothalamus decides the pleuripotent
mesenchymal stem cell differentiation in to an Osteoblast or an Adipocyte. The lineage of both
these cells is common i.e. mesenchymal stem cells.
Abnormal thyroid function at menopause has been proved beyond doubt. The treatment in both
states needs clear understanding. The sub clinical or clinical hypothyroidism is under-treated
and hyperparathyroidism is properly treated.
The weight gain produces a state for demand for calcium. It is a mechanical stress. The bones
are under stress due to increased weight. So even if the serum calcium is normal, here is a
case for calcium supplementation.
This is the reason why FRAX tool (Fracture Risk Assessment) takes BMI (Body mass index) as
an important risk factor for 10 years probability of fracture in post menopausal lady. BMI below
19.5 increases the risk of fractures in future.
A lady, losing weight has no calcium demand, and cannot be helped by any calcium
supplementation. There is no mechanical stress on the bone. She will be more prone for
coronary deposition if calcium supplementations are given.
A heavy build lady may be helped by calcium supplementation but a thin build lady cannot be
helped. Thin build lady has highest chances for developing osteoporotic fractures.
The mechanical demand in a thin lady can be created by weight bearing exercise program.
There you can supplement with calcium.
If we look at the treatment of Osteoporosis, we will find that most (almost all) factors cannot be
modified except BMI.
The factors like age, sex, race, alcohol, and tobacco, corticosteroids, rheumatoid, genetics
(history of factures in parents) and BMD.
Tobacco and alcohol needs only modification of life style. Very difficult and old habits die hard.
There are cultural and social bindings in the western world.
The BMI can be modified. It is dependent on height and weight. Since height cannot be
modified, the weight can be changed. The online FRAX tool will give you an accurate figure
about your 10 years major fractures and fracture at hip risk. Just play with the tool by increasing
or decreasing the figures in weight box.
BMD can be modified by increase in weight or by drugs.
How does Vitamin D work?
Calcium cannot cross a cell barrier without a transport system. The 1,25-dihydroxyvitamin D,
acts to enhance the mRNA to increase synthesis of calcium-binding proteins (calbindin or
cholecalcin), which transport the calcium across the cell barrier to the extra-cellular space.
Vitamin D supplementation will be required only when there is deficiency (dietary or sun
exposure) of vitamin D or calcium. In calcium deficiency status it helps in the mobilization of the
calcium from gut, re-absorption of the calcium and phosphates from kidney and maintains a
normal serum ionic calcium level. There are vitamin D receptors in the skin, muscles, bone, and
at many other places. The principal role of vitamin D in elderly is by increasing the power of
proximal muscles of limb to get better coordination and thus prevent fall.
Who should be treated?
So, for prevention of osteoporosis we do not need calcium and vitamin D in general.
A lady with BMI above 20 does not need any supplementation.
We do need supplementations for correction of deficiency status
We can create mechanical demand by exercises or weight gain, and then we should
supplement with Calcium.